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Cordarone (Amiodarone)

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Cordarone is used to treat a variety of different types of fast, abnormal heart rhythms (these are known as tachyarrhythmias). It is used for severe rhythm disorders when other treatments are not effective or cannot be used.

Other names for this medication:

Similar Products:
Cartia Xt, Lanoxin


Also known as:  Amiodarone.


Cordarone is an antiarrhythmic. It works by stabilizing the heart rhythm in conditions in which the heart is beating too fast or in an irregular rhythm.

Generic name of Cordarone is Amiodarone.

Cordarone is also known as Amiodarone, Pacerone.

Brand name of Cordarone is Cordarone.


Cordarone is best taken with food. However, it is more important to take it consistently with regard to meals. If you take it with food, try to always take it with food to improve absorption of this medicine. If you prefer to take it on an empty stomach, then always try to take it on an empty stomach.

If you want to achieve most effective results do not stop taking Cordarone suddenly.


If you overdose Cordarone and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Cordarone are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Cordarone if you are allergic to Cordarone components.

Do not take Cordarone if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Cordarone if you have complete, second degree, third degree, or severe sinoatrial heart block, an abnormally slow heartbeat, or shock due to serious heart problems, or if you have had fainting due to slow heartbeat (except if you have a pacemaker).

Do not take Cordarone if you are taking cisapride, dofetilide, an H1 antagonist (eg, astemizole, loratadine, terfenadine), an HIV protease inhibitor (eg, ritonavir), a phosphodiesterase type 5 inhibitors (eg, vardenafil), or a streptogramin (eg, dalfopristin, quinupristin).

Lab tests, including electrocardiogram (ECG), chest x-rays, lung tests, liver tests, thyroid tests, and eye exams, may be performed to monitor your progress.

Be careful with Cordarone if you have allergies to medicines, foods, or other substances.

Use Cordarone with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Avoid machine driving.

Try to protect your skin from the sunlight.

Do not stop taking Cordarone suddenly.

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Monitoring of thyroid, liver and pulmonary function tests in patients on amiodarone is less than ideal. This is probably because of lack of awareness of current guidelines.

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High levels of RV pacing are associated with heart failure hospitalization and mortality in a large ICD population. However, ICD patients with some RV pacing (10%-19%) exhibit lower event rates compared with those with very low levels (0-9%), possibly due to the physiologically appropriate nature of that RV pacing.

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Atrial fibrillations in vivo and in vitro were induced by arrhythmogenic drugs. Action potentials were measured by the standard microelectrode technique.

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Amiodarone-associated thyrotoxicosis (AAT) is often poorly tolerated owing to underlying cardiac disease, and it is frequently refractory to conventional medical treatment. The goal of this study was to describe the patient characteristics, management, and outcomes of all the patients treated surgically for AAT at a single institution. We conducted a retrospective chart review of all patients managed surgically for AAT (April 1985 through November 2002) at the Mayo Clinic in Rochester, Minnesota. Altogether, 29 men and 5 women, ages 39 to 85 years (median 60 years), treated with amiodarone for 3 to 108 months underwent near-total or total thyroidectomy. Frequent symptoms were worsening heart failure, fatigue, weight loss, and tremor. Altogether, 12 patients failed medical management of their AAT, and 21 received no preoperative medical therapy. One patient had been successfully managed medically but required definitive treatment. Common indications for operation were the need to remain on amiodarone, cardiac decompensation, medically refractory disease, and severe symptoms, both hyperthyroid and cardiac, necessitating prompt resolution. The median+/-SD American Society of Anesthesiologists (ASA) classification (1 = healthy through 5 = moribund) was 3.00+/-0.58. A total of 27 specimens had histology consistent with AAT. Complications included death (n = 3), rehospitalization (n = 3), symptomatic hypocalcemia (n = 2), pneumonia (n = 2), cervical hematoma (n = 1), prolonged ventilatorywean (n = 1), and stroke (n = 1); one patient developed hypotension, adult respiratory distress syndrome, and sepsis. Of the 31 surviving patients, 25 (80%) remained on amiodarone postoperatively. The median follow-up was 29 months, at which time all surviving patients were free of hyperthyroid symptoms. Thyroidectomy is an effective treatment for AAT but has a high incidence of perioperative morbidity and mortality. The cardiovascular co-morbidities and high operative risk in this group of patients may account for the increased complication rate.

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Serum Tg-Abs were not elevated in any of the studied groups. However, there were significant differences between A and B and also D and other groups (p<0.05). TPO-Abs titers were not elevated in most cases, there were no significant differences between groups. The serum titers of TSHR-Abs were not elevated in any group. We found statistically significant differences between B and D, C and other groups (p<0.05).

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A 22-year-old female, asymptomatic and without any evidence of cardiac disease, was found to have a persistent idioventricular tachycardia (IVT). Sinus rhythm and IVT rates were similar and showed parallel changes in successive resting electrocardiograms. Both IVT and sinus rhythm were transiently slowed or suppressed by vagal stimulation and accelerated by sympathetic stimulation. Long periods of atrial overdrive pacing, at a rate 62% faster than the spontaneous rate of IVT, depressed both ectopic and sinus activity. Fast channel blocking agents (lidocaine, disopyramide), and digoxin and amiodarone failed to modify IVT significantly. Verapamil, a calcium channel blocking drug, allowed total control of the arrhythmia. These electrophysiologic and pharmacologic responses suggest that the IVT may relate to the automatic activity of a ventricular focus of the "slow response" type, functionally resembling an "additional" sinus node with preserved innervation. During an 88-month follow-up, the patient continued to be asymptomatic, warning arrhythmias were never found and the features of IVT remained unmodified.

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Over 300,000 people die of sudden cardiac death (SCD) in the US annually. Implantable cardioverter-defibrillators (ICDs) have been shown to be more effective than antiarrhythmic drugs for the prevention of SCD in specific susceptible populations. Many patients in whom ICDs have been implanted receive concomitant therapy with antiarrhythmic drugs, for the purpose of reducing the frequency of appropriate and inappropriate defibrillation shocks. Drugs may influence defibrillation capacity and therefore influence the function of ICDs. The objective of this article is to review and update the literature regarding the effects of drugs on defibrillation capacity.A literature search was performed using PubMed (1966 to December 2007) to identify clinical studies, case reports and animal studies describing the effects of drugs on defibrillation capacity. Search terms included: antiarrhythmic drugs; cardiovascular drugs; amiodarone; sotalol; flecainide; propafenone; dofetilide; ibutilide; beta-blockers; lidocaine; procainamide; N-acetylprocainamide; mexiletine; disopyramide; moricizine; calcium channel blockers; defibrillation threshold; defibrillation energy requirements; defibrillation energy changes; defibrillation efficacy; implantable cardioverter defibrillators; and external defibrillators. Evidence from clinical studies indicates that amiodarone may increase defibrillation threshold (DFT). In addition, some data indicate that drugs including lidocaine, mexiletine, moracizine (moricizine), verapamil, venlafaxine and anaesthetic agents may increase DFT. In contrast, agents including sotalol, dofetilide and beta-adrenergic receptor antagonists (beta-blockers) may reduce DFT. Propafenone and procainamide appear to have minimal effect on DFT. For those antiarrhythmic drugs with both sodium and potassium channel blockade (e.g. amiodarone), the effect of sodium channel blockade predominates, resulting in an increase in DFT. Numerous drugs may affect defibrillation capacity. These effects must be considered when managing patients who have an ICD and require concomitant pharmacotherapy.

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The phosphodiesterase-5 inhibitors (PDE5i) sildenafil, vardenafil, and tadalafil are considered first-line therapy for the treatment of patients with erectile dysfunction (ED). In addition to the classical pro-erectile-effect, clinical findings have suggested that they can also influence vascular tone in pulmonary, coronary and other vascular tissues, as well as improving symptoms associated with benign prostatic hyperplasia. Therefore, considering the hypothetical widespread application of PDE5i, the potential for drug-drug interactions emerges as a relevant factor in determining the safety profile of PDE5i. Review of relevant literature was conducted using data sources from MEDLINE (1998, to June 2007). The use of nitrates remains the only contraindication for all 3 PDE5i. Vardenafil is also not recommended in patients taking type 1A (such as quinidine, or procainamide) or type 3 antiarrhythmics (such as sotalol, or amiodarone) while no other major limitations have been reported for tadalafil and sildenafil. In contrast to previously reported labeling, recent studies have suggested only a precaution, but not contraindication with the concomitant use of alpha-blockers agents. In addition, precaution is also suggested in the presence of potent CYP3A inhibitors, such as azole antifungals, antiretroviral protease inhibitors, or macrolid antibiotics. This is because sildenafil, vardenafil, and tadalafil are metabolized mainly via the CYP3A4 pathway. On the other hand, statins and testosterone seem to have synergic effects with PDE5i on sexual activity.

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Although the clinical features and onset times vary, amiodarone neuromuscular toxicity manifests as a mixed polyneuropathy, vacuolar myopathy, or both. Creatine kinase levels may not correlate with the degree of myopathy. Variable numbers of lysosomal inclusions in peripheral nerve, endothelial cells, and muscle are characteristic.

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The use of IB in patients receiving amiodarone or propafenone for AFL or AF is equally effective and safe as the use of IB alone. The presence of AFL is the stronger predictor factor for cardioversion.

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Amiodarone has been reported to be a remarkably safe and effective drug in the European and South American experience but American investigators have published conflicting data. Since this disparity may be explained by a different dosing schedule, we prospectively evaluated the safety and efficacy of a low dose regimen in a group of 68 patients with cardiac arrhythmia resistant to conventional therapy, of whom 57 had manifested either ventricular tachycardia or fibrillation. All were loaded either intravenously (17) or orally, and maintained on an oral dose of 200 to 600 mg/day (mean daily dose 317 +/- 114 mg) and followed for 4 to 58 months (22 +/- 11). Results indicated that amiodarone was a safe and effective antiarrhythmic drug when used in lower doses.

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In this study, 37 patients with mean ejection fraction (EF%) of 26.2 (8.2) were included. Myocardial performance was assessed by echocardiography and cardiopulmonary exercise testing. Total tri-iodothyronine (T3), thyroxine, and TSH levels were measured in plasma.

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Persistent atrial fibrillation (AF) is characterized by electrical remodeling, ie, marked decreases in the atrial effective refractory period (ERP), ERP rate adaptation, and atrial conduction velocity. Little information is available on the effects of class III antiarrhythmic drugs on the remodeled atrium. We studied the effects of the class III antiarrhythmic drugs nifekalant, ibutilide, and amiodarone on rate-dependent changes in atrial action potential duration in patients with persistent AF. Right atrial (RA) monophasic action potential duration (MAPD) and intra-atrial conduction time (IACT) were measured at pacing cycle lengths (CLs) of 800, 700, 600, 500, 400, 350, 300, and 250 ms before and after administration of nifekalant (0.4 mg/kg + 0.3 mg/kg/hr, iv), amiodarone (5 mg/kg, iv), or ibutilide (0.01 mg/kg, iv) in 31 patients after successful internal cardioversion of chronic AF of > 2 months duration. Nifekalant and ibutilide significantly increased RA MAPD and the ERP at each CL in a reverse rate-dependent manner. Amiodarone did not affect RA MAPD. Nifekalant did not affect IACT, whereas amiodarone increased IACT at each CL in a rate-dependent manner, and ibutilide increased IACT at CLs ≤ 350 ms. The atrial electrophysiologic effects of the class III antiarrhythmic drugs nifekalant, amiodarone, and ibutilide differ, depending on the degree of electrical and structural remodeling and the effects of the drugs on the depolarizing and repolarizing currents.

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To describe the treatment of persistent supraventricular tachycardia (SVT) in a young horse in endurance training.

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Amiodarone, an efficacious and widely used antiarrhythmic agent, has been reported to cause hepatotoxicity in some patients. To gain insight into the mechanism of this unwanted effect, mice were administered various doses of amiodarone and examined for changes in hepatic histology and gene regulation. Amiodarone induced hepatomegaly, hepatocyte microvesicular lipid accumulation, and a significant decrease in serum triglycerides and glucose. Northern blot analysis of hepatic RNA revealed a dose-dependent increase in the expression of a number of genes critical for fatty acid oxidation, lipoprotein assembly, and lipid transport. Many of these genes are regulated by the peroxisome proliferator-activated receptor-alpha (PPARalpha), a ligand-activated nuclear hormone receptor transcription factor. The absence of induction of these genes as well as hepatomegaly in PPARalpha knockout [PPARalpha-/-] mice indicated that the effects of amiodarone were dependent upon the presence of a functional PPARalpha gene. Compared to wild-type mice, treatment of PPARalpha-/- mice with amiodarone resulted in an increased rate and extent of total body weight loss. The inability of amiodarone to directly activate either human or mouse PPARalpha transiently expressed in human HepG2 hepatoma cells indicates that the effects of amiodarone on the function of this receptor were indirect. Based upon these results, we conclude that amiodarone disrupts hepatic lipid homeostasis and that the increased expression of PPARalpha target genes is secondary to this toxic effect. These results provide important new mechanistic information regarding the hepatotoxic effects of amiodarone and indicate that PPARalpha protects against amiodarone-induced hepatotoxicity.

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Iodine intake is often measured by a surrogate measure, namely urine iodine excretion as almost all ingested iodine is excreted in the urine. However, the methods for urine collection and the reporting of the results vary. These methods, and their advantages and disadvantages, are considered in this article.

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Diabetes mellitus is a risk factor for coronarosclerosis and for high mortality after myocardial infarction (MI). The causes of this high mortality are: more extensive and premature coronarosclerosis, more frequent left ventricular dysfunction, worse glycemic control with increased myocardial oxygen consumption, sulfanylurea drugs before and during MI. The results of a multicenter study (DIGAMI) and other studies suggest that a better control of diabetes using intravenous infusion of insulin and glucose, followed by long-term (3 months) intensive insulin therapy subcutaneously, improves long-term prognosis after MI. The relative reduction of mortality at the end of follow-up (3.4 years) is 28%. Thrombolysis reduces mainly mortality in hospital,s period and does not provoke retinal haemorrhages. Aspirin lowers the relative risk of mortality to 0.72. The beta-blockers are less used in diabetic patients because they probably alter diabetic control, lipid profile and "mask" the hypoglycemic symptoms, but the results of the beta-blocker's effect concerning reduction of mortality are convincing. ACE inhibitors and statins also reduce mortality in diabetics with MI, via beneficial influence of endothelial dysfunction. The ATMA study registers reduction of rhythmogenic mortality by 29% with amiodarone in high risk of arrhythmia after MI. The invasive methods of treatment in diabetes are accompanied by higher risk of reobstruction. The attempt to reduce this tendency is realizable with intracoronary stents, glycoprotein IIb/IIIa inhibitors and aggressive early treatment of all other risk factors.

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Dronedarone is an amiodarone derivative that was approved in the US in July 2009 to reduce the risk of cardiovascular hospitalization in patients with paroxysmal or persistent atrial fibrillation (AF), who are in sinus rhythm (SR), or who will be cardioverted.

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Hyperkalemia is a potentially life-threatening disorder frequently occurring in hospitalized patients. The ischemic myocardium releases potassium into the extracellular space which can cause regional hyperkalemia. These changes may modify the effects of anti-arrhythmic drugs acting on the rapid component of the delayed rectifier potassium current (IKr). We evaluated the influence of increased extracellular potassium concentration [K(+)](e) on IKr inhibition by amiodarone, azimilide, dofetilide, quinidine and sotalol.

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Spontaneous reports in the United States Food and Drug Administration (FDA) Adverse Event Reporting System (AERS) database generated between July 1, 2009, and June 30, 2011.

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Consecutive AIT patients (n = 215) seen at the department of endocrinology of the University of Pisa between 1980 and 2006.

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Ventricular tachycardia (VT) is found usually in patients with structural heart disease. Its symptomatology depends on haemodynamic manifestations. ECG criteria for the diagnosis of VT are known. For the classification of VT we use morphological criteria (monomorphous and polymorphous), duration of arrhythmia (non-and sustained VT) and the pathomechanism of VT (re-entry, increased automation and triggered activity). The clinical impact of VT and the therapeutic approach depend to a great extent on the basic disease. The therapeutic results and prognostic estimates assembled in ischaemic heart disease cannot be mechanically applied in non-ischaemic heart disease. The authors mention the prevalence of VT and the approach to its treatment in dilatative cardiomyopathy, in prolapse of the mitral valve, in hypertrophic cardiomyopathy, in arrhythmogenic right ventricular dysplasia and in patients with a "normal" heart. Only collection of the necessary data and their analysis will help us to achieve better therapeutic results. In the treatment authors focus attention first of all on the pharmacological approach. They emphasize the need of thorough and comprehensive examination of the patient, draw attention to proarrhythmia. In the prevention of relapses of VT most frequently beta-blockers and amiodarone are used (either alone or combined).

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Central cannulation in the fibrinolytic state is associated with a low incidence of important bleeding complications. Thrombolysis should not be withheld in these patients. Cannulation via the subclavian route, however, should be avoided in patients undergoing thrombolysis.

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Cardioversion followed by low-dose amiodarone to maintain normal sinus rhythm appears to be a relatively safe and effective treatment for patients with chronic atrial fibrillation.

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Dronedarone, a multiple ion channel blocker is prescribed for the treatment of paroxysmal and persistent atrial fibrillation. While dronedarone does not precipitate toxicities like its predecessor amiodarone, its clinical use has been associated with idiosyncratic hepatic and cardiac adverse effects and drug-drug interactions (DDIs). As dronedarone is a potent mechanism-based inactivator of CYP3A4 and CYP3A5, a question arose if it exerts a similar inhibitory effect on CYP2J2, a prominent cardiac CYP450 enzyme. In this study, we demonstrated that CYP2J2 is reversibly inhibited by dronedarone (Ki=0.034 μM), amiodarone (Ki=4.8μM) and their respective pharmacologically active metabolites namely N-desbutyldronedarone (NDBD) (Ki=0.55 μM) and N-desethylamiodarone (NDEA) (Ki=7.4 μM). Moreover, time-, concentration- and NADPH-dependent irreversible inactivation of CYP2J2 was investigated where inactivation kinetic parameters (KI, kinact) and partition ratio (r) of dronedarone (0.05 μM, 0.034 min(-1), 3.3), amiodarone (0.21 μM, 0.015 min(-1), 20.7) and NDBD (0.48 μM, 0.024 min(-1), 21.7) were observed except for NDEA. The absence of the characteristic Soret peak, lack of recovery of CYP2J2 activity upon dialysis, and biotransformation of dronedarone and NDBD to quinone-oxime reactive metabolites further confirmed the irreversible inactivation of CYP2J2 by dronedarone and NDBD is via the covalent adduction of CYP2J2. Our novel findings illuminate the possible mechanisms of DDIs and cardiac adverse effects due to both reversible inhibition and irreversible inactivation of CYP2J2 by dronedarone, amiodarone and their active metabolites.

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This is a prospective study of 132 patients, without previous thyroid dysfunction, chronically treated with amiodarone for cardiac arrhythmias, to determine the incidence of thyroid dysfunction. Age was 62 +/- 11 years (mean +/- SD); 54 were female and 78 male. The arrhythmia was supraventricular in 66%, ventricular in 26.5%, and both in 7.5%. Amiodarone dose was 2,390 +/- 65 mg/week, and follow-up 20 +/- 9 months (minimum 9 months). Thyroid status was evaluated at the onset and at regular intervals during follow-up by means of clinical indexes defined by Crooks et al and Billewicz et al. During follow-up 4 patients developed diagnostic indexes (two hyperthyroid and two hypothyroid) and seven more developed suggestive symptoms without reaching a diagnostic index. Biochemical serum determinations of thyroid function proved dysfunction in the four with diagnostic indexes, and were normal in the other seven. The prevalence of new thyroid dysfunction in patients chronically treated with amiodarone in our population is 3%, with equal incidence of hyper and hypofunction. This is the expected incidence for an area with adequate dietary iodine intake. The use of clinical indexes of thyroid dysfunction appear as a useful and economical means of following thyroid function in these patients, saving a large number of biochemical tests.

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Because of the inducible and prolonged VT, despite antiarrhythmic treatment with amiodarone, a cardioverter-defibrillator was implanted (ICD). During threshold measurements of the pacemaker integrated into the ICD the pacemaker impulse was noted to produce a right bundle branch block pattern, the ICD lead having erroneously been placed in the left ventricle via a patent foramen ovale. The lead was left in place, because the ICD was functioning well and lead removal with the possible need of a thoracotomy carried a high risk.

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Although amiodarone is one of the most effective pharmacologic agents used in clinical management of atrial fibrillation (AF), little is known about its differential effects in atrial and ventricular myocardium.

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cordarone 100 tablet 2017-09-11

The aim of the study was to examine the predictive value of N-terminal pro-brain natriuretic peptide (NT-pro-BNP) versus electrophysiologic study in patients with implantable cardioverter-defibrillators (ICDs) after myocardial infarction (MI). We prospectively studied 99 consecutive patients with a history of MI who underwent ICD implantation for primary or secondary prevention of sudden cardiac death. An electrophysiologic study was performed in all patients. Venous blood samples for NT-pro-BNP measurement were obtained at the buy cordarone beginning of the study. The primary end point was ventricular tachycardia or ventricular fibrillation (VT/VF) and the secondary end point was a composite of death, hospitalization for heart failure, or MI. On multivariate Cox regression analysis, NT-pro-BNP level at or greater than median (497 ng/L) was the only significant predictor for VT/VF occurrence (p = 0.047). Along with amiodarone use (p = 0.001), NT-pro-BNP levels higher than median were also associated with a higher risk of composite clinical events (p = 0.036). Kaplan-Meier analysis showed that patients with NT-pro-BNP level at or greater than median had a higher risk of experiencing VT/VF and composite clinical events than patients with NT-pro-BNP levels less than median (log-rank p <0.05). In conclusion, assay of NT-pro-BNP, which is easy to perform and widely available, is superior to electrophysiologic study for prediction of future outcomes in predominantly secondary prophylactic ICD recipients after MI. In the era of primary prophylactic ICD implantation without preimplantation electrophysiologic study, higher NT-pro-BNP levels might help to improve risk-adjusted concomitant antiarrhythmic therapy and device selection.

cordarone medication 2017-02-09

The present paper reviews classification and mode of action of agents that suppress extrasystoles and tachyarrhythmias. These are classified according to their electrophysiological effects observed in isolated cardiac tissues in vitro (Vaughan Williams, 1989). Fast sodium channel blockers (class I) which reduce the upstroke velocity of the action potential are usually subclassified into three groups, class I A-C, according to their effect on the action potential duration. Beta-adrenergic antagonists (class II) exert their effects by antagonizing the electrophysiological effects of beta-adrenergic catecholamines. Class III antiarrhythmic agents (eg amiodarone) prolong the action potential and slow calcium channel blockers (class IV) suppress the calcium inward current and calcium buy cordarone -dependent action potentials. The classification of antiarrhythmic drugs is still under debate. This particularly applies to agents of class I and III. The effect of class I agents is frequency-dependent because the binding affinity of these drugs to the sodium channel is modulated by the state of the channel (modulated receptor hypothesis). Class I agents bind to the channel in the activated and inactivated state and dissociate from the channel in the rested state. This occurs at a drug-specific rate so that class I agents can be subclassified into only two groups, namely in those of the slow- and fast-recovery type respectively (time constant of reactivation greater or smaller than 1 s). Slow-recovery class I agents affect regular action potentials at normal heart rates which can more easily lead to a lengthening of the QRS duration in the ECG, to conduction disturbances and hence to pro-arrhythmic effects.(ABSTRACT TRUNCATED AT 250 WORDS)

cordarone overdose 2017-06-08

Holter ECG recordings were made in 20 patients during AF. One minute ECG segments were selected for analysis. The frequency content of the fibrillatory baseline was then quantified using digital signal processing. After high-pass filtering, the QRST complexes were subtracted using a template matching algorithm. The resulting fibrillatory baseline signal was subjected to Fourier transformation, displayed as a frequency power spectrum and the peak frequency (f) was determined. In 11 patients (7 male, 4 female, age 62 +/- 10 years) 31 paroxysmal AF episodes were analyzed. Duration ranged from 1 min to 665 min (115 +/- 175 min). Initial mean peak f measured 5.1 +/- 0.7 Hz (range 3.9 to 6.9 Hz). There was a positive correlation between f and AF duration (R = 0.53, p = 0.002). AF of less than 15 min duration (n = 13) showed a lower f (4.8 +/- 0.6 Hz) when compared with longer lasting episodes (n = 18, 5.3 +/- 0.7 Hz, p = 0.03). In short AF episodes f was constant, whereas in longer-lasting episodes f increased to 5.8 +/- 0.5 Hz (p < 0.001) within 5 min. In 9 patients (9 male, age 58 +/- 8 years) with persistent AF oral antiarrhythmic drugs (amiodarone n = 5, sotalol n = 3, flecainide n = 1) were given prior to electrical cardioversion buy cordarone for prophylaxis of AF recurrence. Frequency measurements were obtained at baseline and 3 to 5 days after initiation of drug administration. At baseline mean f measured 6.9 +/- 0.4 Hz. Frequency was reduced by antiarrhythmic drugs to 5.8 +/- 0.4 Hz (p < 0.001).

cordarone online 2016-11-30

Iodine-induced thyroid dysfunction will become more important in Austria in the near future, because of the augmentation of the iodine content in salt in 1990. This review therefore tries to summarize the diagnostic and therapeutic problems that may arise in iodine-induced thyroid disease. After discussion of the physiologic reaction of the normal thyroid to iodine the most frequently used iodine-containing drugs used in Austria are presented. Special emphasis is laid on iodine containing antiseptics and on the antiarrhythmic drug amiodarone. The influence of iodine supplementation on the reaction of diseased thyroid glands to iodine overload is stressed. The diagnosis of buy cordarone iodine induced thyroid dysfunction is relatively simple, once it is thought of. Amiodarone-iodine induced thyroid disease may be an exception, because of the intrinsic effect of this drug on thyroid hormone metabolism. Since high intra-thyroidal iodine content inhibits the action of thyrostatics, therapy of iodine-induced hyperthyroidism may be complicated. Alternative possibilities such as cortisone, perchlorate or surgery in thyroid storm are presented. Substitution with 1-thyroxine in iodine-induced hypothyroidism may be harmful in elderly patients with cardiac problems. In conclusion, this review tries to present the state of the art of the solution of diagnostic and therapeutic problems in thyroid dysfunction due to iodine administration.

cordarone drug information 2016-03-14

Data pertaining to the first ICU admission were extracted from the Medical Information Mart for Intensive Care (MIMIC) III database. Patients who received one of the above pharmacologic agents while their heart rate was > 110bpm and had atrial fibrillation documented in the clinical chart were included. Propensity score weighting buy cordarone using a generalized boosted model was used to compare medication failure rates (second agent prior to termination of RVR). Secondary outcomes included time to control, control within 4-hours, and mortality.

cordarone 500 mg 2016-07-24

Dronedarone is superior to placebo but less efficient than amiodarone in maintaining sinus rhythm in patients with a history of AF. In patients with AF and risk factors dronedarone reduces cardiovascular mortality and morbidity, but in patients with buy cordarone severe HF dronedarone significantly increases mortality.

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Several drugs are known to alter thyroid function as a side effect of their primary pharmacological action. Some of these effects have been recognized for decades, but novel thyroid-drug interactions are being recognized as new drugs are developed. buy cordarone It is important for the clinician to be familiar with thyroid-drug interactions, as enhanced surveillance may be necessary in patients undergoing therapies known to affect thyroid function.

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We found no consistent evidence that subclinical hyper- or hypothyroidism contribute to cognitive impairment buy cordarone or decline in old age. Although our data are not in support of treatment of subclinical thyroid dysfunction to prevent cognitive dysfunction in later life, only large randomized controlled trials can provide definitive evidence.

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The optimal approach for acute atrial fibrillation has not been established. Amiodarone is a unique antiarrhythmic agent with activity in both supraventricular and ventricular tachyarrhythmias, but its value for the buy cordarone restoration of sinus rhythm in patients with recent-onset atrial fibrillation has not been demonstrated.

cordarone tablets 200mg 2016-03-04

Ibutilide is a rapid-acting antiarrhythmic drug with worldwide buy cordarone use for conversion of recent-onset atrial fibrillation. Vernakalant, approved in the EU in 2010, is likewise used intravenously, with proven efficacy and safety compared with placebo and amiodarone in randomized clinical trials. The aim of our study was to compare the time to conversion and the conversion rate within 90 min in patients with recent-onset atrial fibrillation treated with vernakalant or ibutilide.

cordarone drug 2016-05-08

The aim of this prospective study was to compare the long-term follow-up after transisthmic ablation of patients with preablation lone atrial flutter, coexistent AF, and drug induced atrial flutter to determine if postablation AF followed a different clinical course and displayed different predictors in these groups. The study evaluated 357 patients who underwent transisthmic ablation for typical atrial flutter. These were divided into four groups according to their preablation history. Group A included patients with typical atrial flutter and without preablation AF (n=120, 33.6%). Group B included patients with preablation AF and spontaneous atrial flutter (n=132, 37.0%). Group C patients had preablation AF and atrial flutter induced by treatment with IC drugs (propafenone or flecainide) (n=63, 17.6%) Group D included patients with preablation AF and atrial flutter induced by treatment with amiodarone (n=42, 11.8%). During a mean follow-up of 15.2 double dagger 10.6 months (range 6-55 months) AF occurred more frequently in groups B (56.1%) and C (57.1%) patients than in groups A (20.8%, P <0.0001) and D (31.0%, P <0.0001) patients. The results of multivariate analysis revealed that different clinical and echocardiographical variables were correlated with postablation AF occurrence buy cordarone in the different groups. Patients with atrial flutter induced by amiodarone have a significantly lower risk of postablation AF than patients with spontaneous atrial flutter and AF, and those with atrial flutter induced by IC drugs. Different clinical and echocardiographical variables predict postablation AF occurrence in different subgroups of patients.

cordarone dose 2015-04-10

One-hour monitoring and bicycle ergometric testing revealed frequent (more than 10 per hour) and complicated buy cordarone ventricular extrasystoles in 105 patients. They were distributed between the treatment and control groups. Long-term treatment with beta-blocking agents reduced the frequency of sudden death and repeated myocardial infarction in the treated group as compared to the controls.

cordarone tab uses 2016-12-12

A series of para-substituted triamterene derivatives (Table 1) were evaluated for their antiarrhythmic properties in vitro. Pharmacological evaluation of the compounds and some class-I- (quinidine, lidocaine, and propafenone) as well as class-III-antiarrhythmic drugs ((+/-)-sotalol and amiodarone) was carried out by measuring the functional refractory period (FRP), the maximal driving frequency (MDF) and the force of myocardial contractions (FC) of electrically stimulated guinea pig buy cordarone atria. The increase in FRP and the decrease in MDF was most pronounced with the class-I-antiarrhythmic drugs, but these compounds showed the typical negative inotropic effects, too. For the class-III-antiarrhythmics only a weak influence on FRP and MDF could be demonstrated, while FC was not altered in the presence of (+/-)-sotalol and amiodarone. Neutral substituted triamterenes like compounds 2-5 as well as most of the benzyltriamterene derivatives showed similar or stronger effects on FRP and MDF as (+/-)-sotalol and amiodarone. With the exception of 4 and 5, these effects were combined with an increase of FC. Compounds 6 and 7, well known-potent diuretics, showed no influence to FRP, MDF and FC. Therefore, we conclude different mechanisms for the antikaliuretic and cardiac activity.

cordarone heart medicine 2015-02-01

Dronedarone has been proposed as one of the first-choice antiarrhythmic drugs for almost all categories of patients with atrial fibrillation Mysoline Drug Interactions . However, its effectiveness in prevention of arrhythmia recurrences is less than that of amiodarone. Administration to patients with severe heart failure is associated with increased mortality and should be avoided. There are also very recent reports over rare but severe cases of hepatic injury in patients treated with dronedarone, including two cases of acute liver failure leading to liver transplant. Intravenous vernakalant is effective for the rapid pharmacological conversion of atrial fibrillation. Dabigatran, an oral direct thrombin inhibitor, has been shown to be effective in stroke reduction without increase in bleeding rates; additionally, no monitoring of antithrombotic effectiveness is needed. Rivaroxaban, an oral direct factor Xa inhibitor, has also shown promising results. These developments in the pharmacological treatment of arrhythmia will presumably affect clinical decision making.

cordarone brand name 2016-07-16

A high-performance liquid chromatographic technique is described for the measurement of amiodarone and its desethyl metabolite in plasma. Preliminary observations are presented on the concentrations of metabolite found during the early stages of chronic amiodarone therapy. A case history is outlined in which noncompliance during treatment with amiodarone was confirmed by measurement of the ratio of desethylamiodarone to Uroxatral Generic Equivalent amiodarone concentrations.

cordarone tab 2016-08-22

Subjects with ischemic cardiomyopathy and hemodynamically tolerated VT were randomized to clinical ablation (n = 60) versus substrate-based ablation that targeted all "abnormal" electrograms in the scar (n = 58). Primary Diflucan 250 Mg endpoint was recurrence of VT. Secondary endpoints included periprocedural complications, 12-month mortality, and rehospitalizations.

cordarone tablet 2016-02-26

IV-amiodarone was administered to 60 patients with ventricular tachyarrhythmia between 2007 and 2012. VT storms, defined as 3 or more episodes of VT within 24 h, occurred in 30 patients (68±12 years, 7 female), with 12 having ischemic and 18 non-ischemic heart disease. We compared the clinical and electrocardiographic characteristics of the patients with VT storms suppressed Allegra 30 Mg by IV-amiodarone (Effective group) to those of patients not affected by the treatment (Refractory group). IV-amiodarone could not control recurrence of VT in 9 patients (30%). The Refractory group comprised 5 patients with acute myocardial infarctions. Although there was no difference in the VT cycle length, the QRS duration of both the VT and premature ventricular contractions (PVCs) followed by VT was narrower in the Refractory group than in the Effective group (140±30 vs. 178±25 ms, P<0.01; 121±14 vs. 179±22 ms, P<0.01). In the Refractory group, additional administration of IV-mexiletine and/or Purkinje potential-guided catheter ablation was effective.

cordarone 5 mg 2015-03-31

The effects of Zoloft Generic Name 200 mg/day of amiodarone were assessed in 18 patients with a history of cardiac failure. Functional class, heart rate, blood pressure, left ventricular ejection fraction, heart size, treadmill exercise tolerance and electrocardiogram were assessed before and eight weeks after the use of amiodarone, and the side effects were monitored.

cordarone y alcohol 2017-07-29

Citrus aurantium extract has been largely used in weight loss and sports performance dietary supplements. However, the safety of C. aurantium-containing products has been questioned mainly due to the association of its use with adverse events in the cardiovascular system. Therefore, this work aimed to assess the potential for herb-drug interactions among a standardized C. aurantium extract (GMP certificate) and amiodarone (narrow therapeutic index drug) in rats. In a first pharmacokinetic study, rats were simultaneously co-administered Priligy Generic Canada with a single-dose of C. aurantium (164 mg/kg, p.o.) and amiodarone (50 mg/kg, p.o.); in a second study, rats were pre-treated during 14 days with C. aurantium (164 mg/kg/day, p.o.) and received amiodarone (50 mg/kg, p.o.) on the 15th day. Rats of the control groups received the corresponding volume of vehicle. Overall, after analysis of the pharmacokinetic data, it deserves to be highlighted the significant increase of the peak plasma concentration of amiodarone in rats pre-treated with C. aurantium extract, while the extent of systemic exposure was comparable between both groups. This paper reports, for the first time, data on the potential of herb-drug interaction between C. aurantium extract and amiodarone. However, specific clinical trials should be performed to confirm these results in humans.

cordarone mg 2016-02-10

Nonsteroidal anti-inflammatory drug (NSAID) use may reduce the incidence of post-cardiothoracic surgery (CTS) atrial fibrillation (AF). The cerebrovascular and cardiovascular safety of using NSAIDs for post-CTS Claritin Dosage Chart AF has not been determined.

cordarone tablets 2017-07-28

The histologic evidence of amiodarone pulmonary toxicity is interstitial pneumonia with foamy alveolar macrophages, which ultrastructurally show lamellar inclusion bodies due to lipid storage. Bronchoalveolar lavage (BAL) fluid findings include foamy macrophages, considered characteristic, and, in certain patients, differential cell counts suggestive of active alveolitis, giving rise to an immunologic explanation for its origin. The present study was undertaken in order to investigate the findings in BAL fluid in nontoxic patients taking amiodarone and to evaluate their clinical relevance. Eleven patients taking amiodarone chlorhydrate for severe ventricular arrhythmias (345 +/- 129 mg/day during 46 +/- 31 months Depakote Pills and an accumulated dose of 440 +/- 337 g) and without clinical or radiological evidences of pulmonary toxicity, were clinically evaluated and studied by BAL. As shown in Table 1, cough and pulmonary rales were common findings (64% and 36% respectively), chest X-Rays were normal or indicative of cardiac failure and arterial blood gases showed slight hypoxemia (PaO2 83 +/- 10). As these are usual findings in advanced cardiac diseases, the patients were considered as having no amiodarone toxicity. BAL was done and the fluid obtained was processed for cytologic study. In every patient foamy macrophages were seen with light microscopy and lamellar bodies were detected by electron microscopy. In 5/10 evaluable patients BAL fluid cell count disclosed an increase in lymphocytes, leukocytes or both, indicative of alveolitis. This group of patient had lower PaO2 and PaO2/PAO2 than "non alveolitic" patients (76 +/- 9 mmHg vs 89 +/- 5 mmHg and 0.72 +/- 0.1 vs 0.85 +/- 0.08 - p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

cordarone 800 mg 2015-05-19

There is still lack of strong evidence, based on systematic studies, that support the relationship between amiodarone Diamox Dosing Pseudotumor use and the risk of acute pancreatitis.

cordarone cost 2015-12-02

No important difference in the decision Topamax 40 Mg making between patients 60 and 80 years old was found. Several individual variables influenced the optimal choice of long term treatment of AF, but not age by itself.

cordarone renal dose 2016-02-08

Although large cohort is required, the present study indicates that Th1/Th2 balance may influence amiodarone metabolism and may be a powerful indicator of amiodarone-induced subclinical lung toxicity Protonix Capsule at least in Japanese.